Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of the literature reflects numerous instances of acute pancreatitis developing in patients while being treated with drugs. The causative relation is not yet definitively established but, in several instances, there appears to be a probable relation. The literature records at least 112 patients with drug-induced acute pancreatitis. Fifty-one instances were caused by steroids or adrenocorticotropic hormone, six by estrogen, two by azathioprine, 16 by diurectics, two by hypercalcemia, 24 by chemotherapy, three by clonidine and phenformin, two by warfarin and one each by salicylate, 1-asparaginase and d-propoxyphene. In addition, many patients have experienced acute pancreatitis while receiving immunosuppressive therapy after renal transplantation.
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PMID:Drug-induced acute pancreatitis. 19 55

Calcium enters the pancreatic juice from two sources, one fraction associated with enzyme protein and another small fraction presumably by diffusion. The calcium concentration in pancreatic juice is lower than in plasma. It decreases with high flow rates and increases asymptotically to plasma concentration with low rates. In chronic pancreatitis calcium concentration is raised in the secretin-stimulated juice. After pancreozymin in moderate chronic pancreatitis it is low but in severe stages of the disease it is high signalling total dissociation from the entrance of enzyme protein, which is very low in these cases. Hypercalcemia stimulates enzyme secretion in the pancreas, hypocalcemia inhibits it. Calcium is essential for intracellular processes associated with secretion, the exact place in the sequence of "stimulus-secretion-coupling" still being unknown. Calcitonin as one of the hormones which regulates calcium homeostasis, inhibits secretion of enzymes but not of fluid and bicarbonate. The action of the parathyroid hormone on the exocrine pancreas is unknown. In primary hyperparathyroidism with chronic hypercalcemia acute and chronic pancreatitis occur 10 to 20 times more frequently than in the general population. In acute pancreatitis of whatever origin hypocalcemia is atypical feature of the disease indicating bad prognosis. The mechanism of its development is still unclear. In chronic pancreatitis the forming of calcified stones in the ducts is typical in cases associated with alcoholism, with protein malnutrition and with primary hyperparathyroidism. But it occurs also in cases with unknown etiology signalling a more general pathophysiological phenomenon. The calcium salts form a precipitate on protein plugs in the juice, which have been observed even in early stages of the disease in the small and larger ducts of the gland.
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PMID:The role of calcium in pancreatic secretion and disease. 77 77

Pancreatitis is seldom seen as a severe complication of renal transplantation. In a review on 1321 renal transplants, 23 cases with 12 deaths are reported (Johnson and Nabseth, 1970). Single case reports may be added. In our departments pancreatitis has proved to be a fairly frequent complication. It developed in 10 (7 percent) of 147 patients with renal transplantation one week to seven and a half years after transplantation (patients with primary hyperparathyroidism excluded). Three of the eight acute cases had haemorrhagic pancreatitis, in two of them leading to death. Two patients had chronic calcifying pancreatitis. Pancreatitis was complicated in one case by abscess formation and in two by severe haemorrhage into a pseudo-cyst. In two patients the diagnosis was made at necropsy only and death was probably not related to the acute pancreatitis. The exact pathogenesis of pancreatitis after renal transplantation cannot be precisely assessed. Possible contributing factors are treatment with corticosteroids, azathioprin, and L-asparaginase, early hypercalcaemia after transplantation, surgery, infections of bacterial or viral origin, and unknown immunological processes.
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PMID:Pancreatitis after renal transplantation. 109 48

The only causal treatment of primary hyperparathyroidism (PHPT) is parathyroidectomy. There are indications in the literature that despite operation expectation of life is shortened because of an increased frequency of cardiovascular and malignant diseases leading to the recommendation for early surgery even in uncomplicated PHPT. It is easier to convince an asymptomatic patient of an operation when he is informed about complications and consequences of an expectative attitude. Therefore, we reviewed our 71 patients operated upon during a 4-year-interval, 58 of whom were followed-up. During 82 operations 115 pathologically altered parathyroid glands were removed. Two persistent paralyses of the recurrent nerve occurred, however, without alteration of the voice. Follow-up of 82% of patients revealed 2 cases of recurrent nephrolithiasis (1 hypercalcaemia, 1 normocalcaemia). Three (5%) true recurrences were found, but neither a pancreatitis nor a peptic ulcer was noted during long-term follow-up. None of the 137 patients operated for a bleeding or perforated peptic ulcer during the last 10 years and 1 of 55 patients with acute pancreatitis during the past 8 years suffered from a PH-PT. However, morbidity and mortality of these two conditions was high. Although correlation to PHPT was low we recommend early operation of PHPT because of the low morbidity rate, zero lethality and reduced expectation of life.
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PMID:[Preventive or therapeutic parathyroidectomy in primary hyperparathyroidism]. 140 51

The low-pressure duct perfusion model reliably produces acute pancreatitis in cats. The main pancreatic duct is made permeable in one of several ways: the perfusion of glycodeoxycholic acid along the main pancreatic duct, the administration of intragastric ethanol, the stimulation of pancreatic secretion into an obstructed duct, or the creation of acute hypercalcemia. Active pancreatic enzymes are then perfused through the main pancreatic duct via a catheter inserted into the duct in the tail of the gland, and acute edematous pancreatitis results. Simultaneous infusion of 16,16-dimethylprostaglandin E2 converts acute edematous into acute hemorrhagic pancreatitis. Histologically, the characteristic changes of human acute pancreatitis are manifest 24 h later: necrosis, polymorphonuclear leukocyte infiltrate, hemorrhage and edema.
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PMID:The low-pressure duct perfusion model of acute pancreatitis. 160 Oct 24

A case of acute pancreatitis associated with primary hyperparathyroidism is reported. There was none of usual causes of pancreatitis, which did not recur following the removal of a parathyroid adenoma. There are over one hundred of cases of acute or chronic pancreatitis associated with hyperparathyroidism in the literature, suggesting a causal relationship between the two entities. The pancreatic disease has been attributed either to the hypercalcemia or to the excess of circulating parathyroid hormone. However, some authors have recently questioned any link between these two diseases.
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PMID:[Acute pancreatitis associated with primary hyperparathyroidism]. 175 Oct 69

Hypercalcemia has been associated with acute pancreatitis clinically and in the experimental animal. We studied the pancreatic ultrastructure in acute experimental hypercalcemia. Anesthetized cats (Pentobarbital, 0.55 mg/kg) received Ca++ (Calcium-Gluconate: 0.6 mmol/kgh; n = 4), K+ (KCl: 1.1 mmol/kgh; n = 4) or NaCl (0.9%; n = 4) locally through retrograde infusion into the splenic artery. Biopsies for electron microscopy (EM) were taken at three hours. Eight cats received intravenous Ca++ (0.6 mmol/kgh, 0.3 mmol/kgh after three hours) or NaCl (0.9%) for 12 hours. Biopsies were collected in two animals in three-hour intervals, and in all animals at twelve hours. After local calcium infusion necrotizing pancreatitis was seen macroscopically in the body of the pancreas. Biopsies for EM showed acinar cell necrosis, hydrops of nuclei and mitochondria and needle-like precipitates in the cytoplasma in the center of calcium perfusion. Biopsies taken from the peripheral region of the macroscopically altered tissue revealed desorganisation of the acinar polarisation and the endoplasmic reticulum, with zymogen granules appearing in the basolateral cell-portion. After intravenous calcium administration no macroscopical changes were seen. In EM acinar cells showed dilatation and proliferation of the golgi apparatus and increased number of condensing vacuoles indicating stimulation. Again, disorganisation of acinar cell polarisation was present. Control animals treated with K+ or NaCl showed normal pancreatic ultrastructure. The morphological changes after calcium infusion indicate direct damage to the acinar cell. Our results suggest that hypercalcemia induced pancreatitis could originate in the acinar cell.
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PMID:[Electron microscopy of the exocrine pancreas in experimental acute hypercalcemia]. 186 39

Metolazone-induced acute pancreatitis and hypercalcemia are described in a 58-year-old woman with severe congestive cardiac failure. Her symptoms and laboratory abnormalities rapidly resolved upon discontinuation of metolazone. Both clinical and laboratory findings make other etiologies for the patient's pancreatitis extremely unlikely. The pathophysiology of thiazide-related hypercalcemia and pancreatitis is reviewed. To our knowledge, neither hypercalcemia nor the combination of acute pancreatitis with hypercalcemia has been reported previously in association with metolazone therapy, and the association of pancreatitis and metolazone has been noted previously only once.
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PMID:Case report: metolazone-associated hypercalcemia and acute pancreatitis. 192 34

We report two cases of adult T-cell leukemia associated with acute pancreatitis and hypercalcemia. After sudden onset of epigastralgia, acute pancreatitis and hypercalcemia were found in both patients. There were no diseases that could explain the acute pancreatitis except for hypercalcemia probably due to adult T-cell leukemia. Thus we considered that hypercalcemia due to adult T-cell leukemia had led to acute pancreatitis. This is the first report of such a complication in adult T-cell leukemia.
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PMID:Two cases of adult T-cell leukemia associated with acute pancreatitis due to hypercalcemia. 195 98

The majority (about 75%) of patients who suffer from acute pancreatitis do so as a consequence of gallstones or alcohol abuse. The other 25% of patients often present difficult diagnostic problems. Over several years the author has accumulated a series of patients with remedial causes of pancreatitis. They include a group of congenital conditions such as pancreas divisum, choledochal cysts and congenital abnormalities of the pancreatic ductal system. Patients who have had pancreatitis and who have an intact gallbladder often have stones that are difficult to identify. Repeated attacks of pancreatitis in the absence of any other apparent cause justifies cholecystectomy, which will often identify the cause so that recurrence can be prevented. A group of nonanatomic causes are also known. They include hyperlipidemia, drugs and toxins, certain systemic illnesses such as systemic lupus erythematosus, pregnancy, hypercalcemia, hereditary causes and occasionally cancer. In his lecture the author reviews the various etiologies of acute pancreatitis and describes an algorithm that can be used when the diagnosis is difficult.
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PMID:Recurrent acute pancreatitis--rarely idiopathic: 1989 Du Pont lecture. 226 8


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